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Companion Animals: Vitamin K
Deficiency

The major clinical sign of vitamin K deficiency in all species is impairment of blood coagulation (Griminger, 1984). Other clinical signs include low prothrombin levels, increased clotting time and hemorrhaging. In its most severe form, a lack of vitamin K will cause subcutaneous and internal hemorrhages, which can be fatal. Vitamin K deficiency can result from dietary deficiency, lack of microbial synthesis within the gut, inadequate intestinal absorption or inability of the liver to use the available vitamin K. Accidental dicumarol, or warfarin, poisoning should be considered in dogs or cats observed with hemorrhagic syndromes.

Measurement of clotting time or prothrombin has been used to evaluate the body status of vitamin K and is considered a fairly good measure of vitamin K deficiency. Prolongation of the clotting time in the absence of liver disease indicates vitamin K deficiency. Further clarification of a deficiency can be provided by assays for specific vitamin K-dependent factors or by the rapid response to administration of vitamin K. The currently available method for measuring the inadequacy of vitamin K intake is to measure the plasma concentration of one of the vitamin K-dependent clotting factors, prothrombin (factor II), factor VII, factor IX, or factor X (Suttie, 1984). In experimentally induced dicumarol poisoning, "hemorrhagic sweet clover disease," Alstad et al. (1985) reported that normal prothrombin time is equal to or less than 20 seconds. Deficiency of vitamin K was characterized by prothrombin times greater than 40 to 60 seconds; with severe deficiency, prothrombin time can be as long as 5 to 6 minutes.
A. Deficiency in Dogs

Vitamin K deficiency signs are only occasionally described for dogs; however, accidental intake of dicumarol types of rat poison such as warfarin and diphenadione (vitamin K antagonist) will result in a hemorrhagic condition in dogs (Kerr, 1986; Mount and Kass, 1989). Clinical signs in dogs include paleness and evidence of slow but persistent bleeding from a number of sites including gums, bowel, and several injection punctures (Kerr, 1986). Prothrombin time was 7.5 minutes compared to 10 seconds after six injections with vitamin K. Dicumarol also induces liver parenchymal cell ultrastructural changes (Barnhart et al., 1964), such as collapse of membranous elements of the endoplasmic reticulum around the mitochondria and reduced cytoplasmic ribosome concentration.

Vitamin K deficiency characterized by excessive bleeding was reported in a Boston terrier with bile and cystic duct obstructions (Neer and Hedlund, 1989). The deficiency has also been induced experimentally by biliary diversion; dogs developed depressed levels of plasma prothrombin and exhibited massive hemorrhage (Quick et al., 1962). Vitamin K absorption from both diet and intestinal bacterial synthesis was apparently reduced. Some reports indicate that newborn pups suspected of vitamin K deficiency sometimes respond to vitamin K therapy.
B. Deficiency in Cats

Vitamin K deficiency is rare in cats. However, vitamin K antagonism attributable to ingestion of rodenticides containing warfarin or related compounds is a cause of hemorrhaging in cats. Clinical signs of vitamin K deficiency could include hematomas in the elbows, hemorrhage in the conjunctiva, extensive hemorrhage in and around the stifle joint, with necropsy revealing extensive hemorrhage in the bladder, sublumbar area, pelvic canal and perineum (Maddison et al., 1990).

Vitamin K is fat soluble, and fat malabsorption may result in a deficiency in cats (Green 1983; Prentice, 1985). Vitamin K deficiency associated with fat malabsorption attributable to exocrine pancreatic insufficiency has been reported in a cat (Perry et al., 1989).

Apparent genetic abnormalities may bring about vitamin K deficiencies in cats. A complex coagulation failure, which includes factor X deficiency, has been observed in Devon Rex cats in the United Kingdom (Evans, 1985; Littlewood et al., 1995), and a possibly similar abnormality has been described in a family of boxers (Dodds, 1981). Maddison et al. (1990) suggested that vitamin K-dependent hemorrhaging in Devon Rex cats in Australia could be due to malabsorption of vitamin K or possibly to a defective epoxide reductase activity. In the condition there are marked reductions in factors II, VII, IX and X, the vitamin-K dependent coagulation factors. This genetic effect appears to be inherited as an autosomal trait.

 
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